Urinary hepcidin: an inverse biomarker of acute kidney injury after cardiopulmonary bypass?

Purpose of review In this review, we discuss the potential role of urinary hepcidin, a 2.8-kDa hormonal regulator of iron metabolism, as a biomarker of acute kidney injury (AKI) after cardiopulmonary bypass. Recent findings Hepcidin is one of the novel biomarkers of AKI that have been identified using hypothesis-free, proteomic analysis of urine or plasma in patients who develop AKI. Collectively, these markers promise a new era for the early diagnosis and treatment of AKI in the ICU and an understanding of their biological role may also provide mechanistic insights into the pathogenesis of AKI. Although data confirming the association between urinary hepcidin and AKI are as yet limited, we believe hepcidin is of particular interest because hepcidin may be a biomarker specific to cardiopulmonary bypass-associated AKI; as a central regulator of iron metabolism, hepcidin could play a biological role in the pathogenesis of AKI after cardiopulmonary bypass; and hepcidin displays an intriguing negative association with AKI, in that a smaller increase in hepcidin from baseline after cardiopulmonary bypass appears to predict greater chance of developing AKI. Summary Smaller increases in urinary hepcidin, a central regulator of iron metabolism, may be associated with greater risk of AKI after cardiopulmonary bypass. Further research is required to establish the significance and nature of this association.